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Mechanisms for the coupling of cannabinoid receptors to intracellular calcium mobilization in rat insulinoma beta-cells.
Exp Cell Res. 2007 Aug 15; 313(14):2993-3004.EC

Abstract

In RIN m5F rat insulinoma beta-cells, agonists at cannabinoid CB(1) receptors modulate insulin release. Here we investigated in these cells the effect of the activation of cannabinoid CB(1) and CB(2) receptors on intracellular Ca(2+) ([Ca(2+)](i)). The CB(1) agonist arachidonoyl-chloro-ethanolamide (ACEA), and the CB(2) agonist JWH133, elevated [Ca(2+)](i) in a way sensitive to the inhibitor of phosphoinositide-specific phospholipase C (PI-PLC), U73122 (but not to pertussis toxin and forskolin), and independently from extracellular Ca(2+). PI-PLC-dependent Ca(2+) mobilization by ACEA was entirely accounted for by activation of inositol-1,3,4-phosphate (IP(3)) receptors on the endoplasmic reticulum (ER), whereas the effect of JWH133 was not sensitive to all tested inhibitors of IP(3) and ryanodine receptors. ACEA, but not JWH133, significantly inhibited the effect on [Ca(2+)](i) of bombesin, which acts via G(q/11)- and PI-PLC-coupled receptors in insulinoma cells. The endogenous CB(1) agonists, anandamide and N-arachidonoyldopamine, which also activate transient receptor potential vanilloid type 1 (TRPV1) receptors expressed in RIN m5F cells, elevated [Ca(2+)](i) in the presence of extracellular Ca(2+) in a way sensitive to both CB(1) and TRPV1 antagonists. These results suggest that, in RIN m5F cells, CB(1) receptors are coupled to PI-PLC-mediated mobilization of [Ca(2+)](i) and might inhibit bombesin signaling.

Authors+Show Affiliations

Endocannabinoid Research Group, Institute of Cybernetics, National Research Council, Via Campi Flegrei 34, Comprensorio Olivetti, 80078 Pozzuoli, Naples, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17585904

Citation

De Petrocellis, Luciano, et al. "Mechanisms for the Coupling of Cannabinoid Receptors to Intracellular Calcium Mobilization in Rat Insulinoma Beta-cells." Experimental Cell Research, vol. 313, no. 14, 2007, pp. 2993-3004.
De Petrocellis L, Marini P, Matias I, et al. Mechanisms for the coupling of cannabinoid receptors to intracellular calcium mobilization in rat insulinoma beta-cells. Exp Cell Res. 2007;313(14):2993-3004.
De Petrocellis, L., Marini, P., Matias, I., Moriello, A. S., Starowicz, K., Cristino, L., Nigam, S., & Di Marzo, V. (2007). Mechanisms for the coupling of cannabinoid receptors to intracellular calcium mobilization in rat insulinoma beta-cells. Experimental Cell Research, 313(14), 2993-3004.
De Petrocellis L, et al. Mechanisms for the Coupling of Cannabinoid Receptors to Intracellular Calcium Mobilization in Rat Insulinoma Beta-cells. Exp Cell Res. 2007 Aug 15;313(14):2993-3004. PubMed PMID: 17585904.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms for the coupling of cannabinoid receptors to intracellular calcium mobilization in rat insulinoma beta-cells. AU - De Petrocellis,Luciano, AU - Marini,Pietro, AU - Matias,Isabel, AU - Moriello,Aniello Schiano, AU - Starowicz,Katarzyna, AU - Cristino,Luigia, AU - Nigam,Santosh, AU - Di Marzo,Vincenzo, Y1 - 2007/05/18/ PY - 2007/02/06/received PY - 2007/04/07/revised PY - 2007/05/01/accepted PY - 2007/6/26/pubmed PY - 2007/12/6/medline PY - 2007/6/26/entrez SP - 2993 EP - 3004 JF - Experimental cell research JO - Exp Cell Res VL - 313 IS - 14 N2 - In RIN m5F rat insulinoma beta-cells, agonists at cannabinoid CB(1) receptors modulate insulin release. Here we investigated in these cells the effect of the activation of cannabinoid CB(1) and CB(2) receptors on intracellular Ca(2+) ([Ca(2+)](i)). The CB(1) agonist arachidonoyl-chloro-ethanolamide (ACEA), and the CB(2) agonist JWH133, elevated [Ca(2+)](i) in a way sensitive to the inhibitor of phosphoinositide-specific phospholipase C (PI-PLC), U73122 (but not to pertussis toxin and forskolin), and independently from extracellular Ca(2+). PI-PLC-dependent Ca(2+) mobilization by ACEA was entirely accounted for by activation of inositol-1,3,4-phosphate (IP(3)) receptors on the endoplasmic reticulum (ER), whereas the effect of JWH133 was not sensitive to all tested inhibitors of IP(3) and ryanodine receptors. ACEA, but not JWH133, significantly inhibited the effect on [Ca(2+)](i) of bombesin, which acts via G(q/11)- and PI-PLC-coupled receptors in insulinoma cells. The endogenous CB(1) agonists, anandamide and N-arachidonoyldopamine, which also activate transient receptor potential vanilloid type 1 (TRPV1) receptors expressed in RIN m5F cells, elevated [Ca(2+)](i) in the presence of extracellular Ca(2+) in a way sensitive to both CB(1) and TRPV1 antagonists. These results suggest that, in RIN m5F cells, CB(1) receptors are coupled to PI-PLC-mediated mobilization of [Ca(2+)](i) and might inhibit bombesin signaling. SN - 0014-4827 UR - https://www.unboundmedicine.com/medline/citation/17585904/Mechanisms_for_the_coupling_of_cannabinoid_receptors_to_intracellular_calcium_mobilization_in_rat_insulinoma_beta_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(07)00221-2 DB - PRIME DP - Unbound Medicine ER -